Multiple sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system which usually presents in the form of recurrent attacks of focal or multifocal neurologic dysfunction. Attacks occur, remit, and recur, seemingly randomly over many years. Remission is often incomplete and as one attack follows another, a stepwise downward progression ensues with increasing permanent deficit.
Clinical disease is associated with blood-brain barrier dysfunction; infiltration of the central nervous system by mononuclear cells, mainly macrophages and T lymphocytes, and serum products; and demyelination (Harris J. O., et al., Ann. Neurol. 29:548 (1991); Kermonde A. G., et al., Brain 113:1477 (1990)).
Presently the nature of autoantigens responsible for multiple sclerosis is not known, nor is the action which triggers the autoimmune response. One popular theory involves the similarity of a viral protein to a self antigen, which results in autoreactive T cells or B cells recognizing a self antigen. Whereas B-lymphocytes produce antibodies, thymus-derived or "T-cells" are associated with cell-mediated immune functions. T-cells recognize antigens presented on the surface of cells and carry out their functions in association with "antigen-presenting" cells.
Currently no practical and efficacious treatments for multiple sclerosis exist. Thus, the development of a method for treating multiple sclerosis would be of immense benefit.